KANSL2 is a non-catalytic component of the NSL histone acetyltransferase complex that mediates histone H4 acetylation at lysine residues to promote transcription initiation 1. Beyond transcriptional regulation, KANSL2 maintains nuclear architecture stability through MOF-dependent acetylation of lamin A/C, with deficient acetylation leading to impaired nuclear mechanostability and genomic instability including chr12 2. KANSL2 also regulates intraciliary transport genes necessary for cilium assembly and microtubule cytoskeleton organization [UniProt reference]. Disease relevance spans multiple cancer types: KANSL2 is essential for triple-negative breast cancer and prostate cancer cell fitness 3, regulates pancreatic ductal adenocarcinoma invasion independently of proliferation 4, and promotes glioblastoma stemness and tumorigenesis through POU5F1-dependent pathways 5. Ropivacaine suppresses glioblastoma growth partly through the miR-21-5p/KANSL2 axis 6. Clinically, TAF4A-dependent KANSL2 expression is critical for muscle stem cell quiescence and skeletal muscle regeneration 7. Additionally, genetic variants in the KANSL2 region associate with reading disability and overlap with neurodevelopmental disorders including ADHD and autism spectrum disorder 8.